Engineered viruses rebuild heartbeat

Using viruses to deliver a single gene, U.S. researchers have reprogrammed heart cells and converted them into working biological pacemakers that could regulate the erratic beating of a failing heart.

The research, at the Cedars-Sinai Heart Institute, focused on the gene Tbx18, which is involved in the development of the sinoatrial node, the heart's natural pacemaker. Cells in the sinoatrial node create the orderly and rhythmic healthy heartbeat by generating waves of electrical activity. If this goes wrong, the heart can beat erratically, either too fast or too slowly, and need the support of an electronic pacemaker to keep it in line.

In studies on the bench, introducing the gene using a virus transformed normal heart cells into cells that looked and behaved like sinoatrial node cells. And in guinea pigs with heart disease, using the virus to transform cells in situ in the heart triggered pacemaker activity and corrected the erratic heartbeat. The research has been published online in Nature Biotechnology.

"Although we and others have created primitive biological pacemakers before, this study is the first to show that a single gene can direct the conversion of heart muscle cells to genuine pacemaker cells. The new cells generated electrical impulses spontaneously and were indistinguishable from native pacemaker cells," said Hee Cheol Cho, a Heart Institute research scientist, in a press release.

Talking to BBC News, Cho explained that the research used a human gene, so he expected that the process would work in the same way in humans.

This has only been tested in actual guinea pigs so far. However, if it makes it through the development process into human "guinea pigs," potentially as a gene therapy to convert a targeted cluster of cells in the heart, or transplanted engineered cells into the heart muscle, it could have potential to replace or at least provide an alternative to surgically implanted electronic pacemakers.

- read the press release
- see the abstract
- check out the article in BBC News